Ethanol-induced changes in blood pressure, vasoreactivity and platelet aggregation may have common etiologies which include the disruption of prostaglandin metabolism and catecholamine secretion. Ethanol has been shown to markedly alter omega-6 fatty acid levels, prostaglandin metabolism, and catecholamine levels in the cardiovascular system. Prostaglandins such as prostacyclin (PGI2) and thromboxane (TXA2), and also catecholamines such as epinephrine (E) and norepinephrine (NE) are active in the cardiovascular system and may play a role in the pathophysiology associated with ethanol consumption. Using our automated apparatus for precise control of inhalation chamber ethanol vapor and blood ethanol concentrations, the effects of a range of ethanol doses on vascular tone and reactivity, platelet aggregation, fatty acid content, prostaglandin production and plasma catecholamine levels were determined in the rat. Acute exposure to moderate blood ethanol concentrations (BEC) was associated with increased vascular production of PGI2 and plasma catecholamines, whereas platelet production of TXA2 decreased. Blood pressure is elevated in these animals, however, platelet aggregation and the pressor effect of norepinephrine (NE) were mildly decreased. Chronic exposure to high BEC is associated with a dramatic reduction in vascular and platelet prostaglandin (PG) production and a slight increase in plasma catecholamine levels. Concentrations of fatty acid precursors to PGs were reduced by as much as 50% in the lipid extracts of these preparations. Blood pressure is generally reduced in these animals and platelet aggregation decreases dramatically, however, the pressor effects of TXA2 and NE were significantly increased. Long-term ethanol exposure did not induce a reduction in fatty acid precursors of PGs or the capacity to produce 2-series PG in animals fed a diet rich in gamma-linolenic acid (20:3).